BACKGROUND: Pulmonary hypertension is a postoperative complication that may adversely affect the outcome of lung transplantation. The effect of nitric oxide (NO) inhalation on pulmonary hemodynamic indices after lung transplantation was studied and compared with findings in control pigs. METHODS: Varying concentrations of NO were inhaled by 5 pigs after left lung transplantation and right pneumonectomy and by 5 controls after right pneumonectomy at an inspired oxygen fraction of 0.21 and 0.5. Hemodynamic data were recorded continuously, and fast circulatory courses were analyzed. RESULTS: Inhalation of NO reduced pulmonary vascular resistance and mean pulmonary arterial pressure in all pigs, but the decrease was pronounced and dose dependent only at an inspired oxygen fraction of 0.21 in the pigs that had transplantation. These were the only pigs that became hypoxic. With the termination of NO, there was a dose-independent rebound pulmonary vasoconstriction in the controls, especially at an inspired oxygen fraction of 0.21, but not in the pigs that had transplantation. This response was transient and could be blunted with a higher inspired oxygen fraction. CONCLUSION: Inhalation of NO reduced pulmonary vascular resistance in the transplanted lung and may be useful in the treatment of pulmonary hypertension after lung transplantation. The rebound pulmonary vasoconstriction with the termination of NO inhalation stresses the need to be aware of this effect and to wean NO carefully in clinical situations. This study showed oxygen dependency, which has to be taken into consideration in dose-response studies involving NO inhalation.
BACKGROUND:Pulmonary hypertension is a postoperative complication that may adversely affect the outcome of lung transplantation. The effect of nitric oxide (NO) inhalation on pulmonary hemodynamic indices after lung transplantation was studied and compared with findings in control pigs. METHODS: Varying concentrations of NO were inhaled by 5 pigs after left lung transplantation and right pneumonectomy and by 5 controls after right pneumonectomy at an inspired oxygen fraction of 0.21 and 0.5. Hemodynamic data were recorded continuously, and fast circulatory courses were analyzed. RESULTS: Inhalation of NO reduced pulmonary vascular resistance and mean pulmonary arterial pressure in all pigs, but the decrease was pronounced and dose dependent only at an inspired oxygen fraction of 0.21 in the pigs that had transplantation. These were the only pigs that became hypoxic. With the termination of NO, there was a dose-independent rebound pulmonary vasoconstriction in the controls, especially at an inspired oxygen fraction of 0.21, but not in the pigs that had transplantation. This response was transient and could be blunted with a higher inspired oxygen fraction. CONCLUSION: Inhalation of NO reduced pulmonary vascular resistance in the transplanted lung and may be useful in the treatment of pulmonary hypertension after lung transplantation. The rebound pulmonary vasoconstriction with the termination of NO inhalation stresses the need to be aware of this effect and to wean NO carefully in clinical situations. This study showed oxygen dependency, which has to be taken into consideration in dose-response studies involving NO inhalation.